1. Field of the Invention
The present invention relates generally to tissue treatment systems and in particular to the stimulation of cartilage formation using reduced pressure treatment
2. Description of Related Art
Clinical studies and practice have shown that providing a reduced pressure in proximity to a tissue site augments and accelerates the growth of new tissue at the tissue site The applications of this phenomenon are numerous, but application of reduced pressure has been particularly successful in treating wounds. This treatment (frequently referred to in the medical community as “negative pressure wound therapy,” “reduced pressure therapy,” or “vacuum therapy”) provides a number of benefits, including faster healing and increased formulation of granulation tissue. Typically, reduced pressure is applied to tissue through a porous pad or other manifolding device. Unless otherwise indicated, as used herein, “or” does not require mutual exclusivity. The porous pad, often an open-cell foam, contains cells or pores that are capable of distributing reduced pressure to the tissue and channeling fluids that are drawn from the tissue. The porous pad often is incorporated into a dressing having other components that facilitate treatment. While reduced pressure therapy has been used to treat soft tissue injuries, such therapy has not been used extensively to promote, for example, cartilage regeneration.
Damage to cartilage through age, injury, wear, and metabolic disorders, such as osteoarthritis, affect millions of people throughout the world. Indeed, it is currently believed that 85% of all Americans will develop degenerative joint disease as a result of normal activities that damage cartilage. The gradual degeneration and destruction of articular cartilage, one of three different types of cartilage, may be due to trauma, structural deformation of the joints and being overweight. Articular cartilage is a highly organized avascular tissue composed of chondrocytes formed in an extracellular matrix. Articular cartilage is generally thin with an extremely low or insignificant blood flow and, as such, has a very limited ability to repair or heal itself Partial-thickness chondral defects, for example, cannot spontaneously heal. This tissue is extremely important to the normal, healthy function and articulation of joints. Articular cartilage enables joint motion surfaces to articulate smoothly with a very low coefficient of friction. It also acts as a cushion to absorb compressive, tensile, and shearing forces and, thus, helps protect the ends of bone and surrounding tissue. The clinical manifestations of cartilage damage or wear are often painful and debilitating, including swelling of the joint, crepitation, and decrease in functional mobility. As the condition worsens, pain may even limit minimum physical efforts and persist at rest making it difficult to sleep. If the condition persists without correction and/or therapy, the joint can be totally destroyed, leading the patient to major replacement surgery with a total prosthesis, or to disability. The complications of cartilage injury are multifold. For example, injured cartilage tends to cause additional damage to articulations and the articular surfaces. Damage to articular surfaces is linked to bone spur development, which further limits joint movement.
The other two types of cartilage are fibrocartilage and elastic cartilage. Fibrocartilage offers strength with flexibility while providing shock absorption against impact and tensile forces. Fibrocartilage may be found in several areas of the body including, the annulus fibrosus of the intervertebral discs and the meniscus located in the knee joint. Elastic cartilage may provide flexibility and structural support to portions of the body. Elastic cartilage may also be found in several areas of the body including, the outer ear, the larynx, and the epiglottis. Fibrocartilage and elastic cartilage may also be damaged from injuries or degeneration. The damaged cartilage may be painful and debilitating and may further result in cosmetic defects. Consequently, damaged cartilage can have sweeping effects on the body that may ultimately lead to a reduced quality of life.
Typically, the body cannot completely repair the cartilage. Cartilage is primarily composed of collagen fibers, proteoglycans and elastin fibers that form an extracellular matrix. The matrix is formed by specialized cells called chondrocytes. Chondrocytes are one of the few cell types that can survive with a minimal blood supply. However, when cartilage is damaged, the lack of an adequate blood supply to the chondrocytes results in an inability to regenerate new chondrocytes, a process that requires an increased amount of nutrients and access through the blood stream to other cells and proteins. Full thickness articular cartilage damage that exposes the subchondral bone or osteochondral lesions may generate a normal inflammatory response that repairs the cartilage, but the new fibrocartilage formation is functionally inferior.
Current techniques to inhibit or delay degeneration of joint cartilage include use of anti-inflammatory agents, chondrogenic stimulating factors, antirheumatics, systemics, viscoprotection and injection of depot steroids. Other methods to inhibit or delay degeneration of joint cartilage include implantation of chondrocytes or synthetic matrices. One method of treatment for cartilage damage is surgical intervention, with reattachment and reconstruction of the damaged tissue. None of the above methods are totally satisfactory, and those methods rarely restore full functionality or return the tissue to its native normal state. In addition, none of those methods are proven to regenerate cartilage in situ and in vivo.